Approach Considerations

The American Association of Sleep Medicine (AASM) guideline states that the 2 primary goals of treatment are to improve sleep quality and to improve related daytime impairments.
[1] Strategies for achieving these goals will vary depending on the underlying etiology. If the patient has a medical, neurologic, or sleep disorder, treat the disorder. In particular, adequate pain control can greatly relieve the insomnia associated with pain syndromes. In 2017, the AASM released an updated guideline for the pharmacologic treatment of chronic insomnia in adults.
[6]

The AASM guideline recommends psychological and behavioral interventions (including, but not limited to, cognitive-behavioral therapy [CBT]) as effective in the treatment of chronic comorbid insomnia as well as primary insomnia. The guideline also encourages these interventions as initial therapy when appropriate.
[1]

The treatment of primary (psychophysiologic) insomnia begins with education about the sleep problem and appropriate sleep hygiene measures (elements of good sleep hygiene are described in Patient Education). Before therapy is instituted, most patients are asked to maintain a sleep diary for 1-2 weeks (see Sleep Diary). This provides a clearer picture of the degree of sleep disturbance and allows development of a tailored treatment.

Strong evidence supports the use of nonpharmacologic interventions (eg, CBT) for insomnia. Head-to-head comparison has shown that the long-term benefits of nonpharmacologic interventions are superior to those of medication.
[67, 68, 69] CBT is now considered the most appropriate treatment for patients with primary insomnia.
[3, 4, 5] Use of this therapy is based on the fact that primary insomnia is associated with physiologic, emotional, and cognitive arousal and conditioning to arousal in bed.

If the patient has a psychiatric disorder, the disorder should be treated. Management may involve medications, psychotherapy, and possible referral to a psychiatrist, psychologist, or therapist. If the insomnia is related to medication or drug abuse, the offending medication or drug must be slowly tapered and withdrawn.

Even when comorbid causes of insomnia (ie, medical, psychiatric) are treated, however, variable degrees of insomnia persist that require additional interventions. These patients can benefit from CBT
[16] and a short course of a sedative-hypnotic or melatonin receptor agonist. In the case of a psychiatric disorder (eg, depression
[70] or anxiety), CBT and a short-term sedative-hypnotic in conjunction with an antidepressant can be beneficial.

Next:

Cognitive-Behavioral Therapy

Cognitive-behavioral therapy (CBT) can be used to ameliorate factors that perpetuate or exacerbate chronic insomnia, such as poor sleep habits, hyperarousal, irregular sleep schedules, inadequate sleep hygiene, and misconceptions about sleep. CBT is most effective for primary insomnia, but it is also effective for comorbid insomnia as adjunctive therapy.
[1]

Multiple randomized, controlled trials have demonstrated the efficacy of CBT. Sleep latency, total sleep time, duration of wakefulness, and sleep quality have been shown to improve with CBT. From 50-75% of patients attain clinically significant improvement. CBT also improves the absolute amount of slow-wave sleep by 30%. Six-month follow-up has shown sustained efficacy for this treatment modality.

The American Academy of Sleep Medicine (AASM) evidence-based practice parameter found that CBT (all components), as well as individual components of stimulus-control, paradoxical intention, relaxation training, and biofeedback, were effective.
[4] CBT has also been shown to be better in weaning patients from hypnotics than tapering medications alone.

Limitations of CBT are that providers must be trained in its use and that the technique is time consuming. Most studies of CBT used trained psychologists to work with patients for an average of 5.7 sessions over 6.5 weeks, with each session lasting at least 20-40 minutes. A study by Edinger et al showed that a total of 4 biweekly individual treatments represents the optimal dosing of CBT.
[71] Obviously, this would not be practical for most primary care providers or neurologists. In addition, it is currently not known how effective CBT can be when administered by a nonpsychologist.

Some sleep centers have behavioral medicine specialists who can administer CBT. Preliminary evidence by Morin indicated that providing written information about CBT can be helpful.
[73] An Internet-based CBT learning program for patients is also available for a nominal cost (see CBTforINSOMNIA.com).

The components of CBT include the following:

Sleep hygiene education

Cognitive therapy

Relaxation therapy

Stimulus-control therapy

Sleep-restriction therapy

CBT for insomnia (CBT-I) is a term for the combination of cognitive therapy and behavioral therapy, such as stimulus-control therapy or sleep-restriction therapy (with or without relaxation therapy).
[1]

The 2008 AASM guideline recommends including at least one behavioral intervention in initial treatment. Multicomponent therapy that includes behavioral therapy without cognitive therapy is also recommended in the treatment of chronic insomnia.
[1]

Sleep hygiene education

Sleep hygiene education addresses behaviors that are incompatible with sleep. These include caffeine or alcohol use, environmental noise, inappropriate room temperature, and watching TV in bed. The 2008 AASM guideline recommends adherence to sleep hygiene rules for all patients with chronic insomnia but finds insufficient evidence of effectiveness when following these sleep hygiene rules as monotherapy and, thus, advises its use as adjunctive therapy.
[1]

Cognitive therapy and relaxation therapy

In cognitive therapy, the patient is educated to correct inaccurate beliefs about sleep and to reduce catastrophic thinking and excessive worrying about the consequences of failing to obtain adequate sleep.

Relaxation therapy comprises several techniques. In progressive relaxation, the patient is taught to recognize and control tension through a series of exercises that consist of first tensing and then relaxing each muscle group in a systematic way. Guided imagery and meditation teach the patient how to focus on neutral or pleasant targets in place of racing thoughts. Biofeedback techniques can also be used. These techniques have the advantages of providing patients with immediate feedback regarding their level of tension and rapidly teaching them how to relax.

Stimulus-control therapy

Stimulus-control therapy works to reassociate the bed with sleepiness instead of arousal. Rules for its use include the following:

Use the bed only for sleeping and sexual activity (no reading, TV, eating, or working in bed)

Go to bed only when sleepy

If unable to fall asleep in 15-20 minutes, get out of bed to do something relaxing until sleepy; this can be repeated as often as needed

Do not spend more time in bed than is needed by establishing a standard wake-up time

Refrain from daytime napping

Sleep-restriction therapy

Sleep-restriction therapy is based on the fact that excessive time in bed often perpetuates the insomnia. Limiting the time spent in bed leads to more efficient sleep that is both consolidated and more regular and predictable. Time in bed is allowed to increase as the patient demonstrates a continuing ability to sleep in an efficient and consolidated manner.

This treatment plan consists of limiting time in bed to the patient's estimated total sleep time (not less than 5 hours) and increasing it by 15-30 minutes for a given week when the patient estimates that his or her sleep efficiency (SE; ratio of time asleep to time in bed) has reached greater than 85%. The amount of time in bed remains the same when the SE falls between 80 and 85% and is decreased by 15-30 minutes for a given week when the SE is less than 80%. Periodic (weekly) adjustments are made until the optimal sleep duration is achieved.

Use sleep-restriction therapy with caution in patients with occupations for which sleep deprivation can have devastating consequences. These include commercial truck drivers, operators of heavy machinery, and pilots.

Efficacy of CBT versus sedative-hypnotics for primary insomnia

Several randomized trials comparing CBT against hypnotics for primary insomnia have been published. Morin and colleagues compared temazepam with CBT in older patients and found similar short-term effects, but there was continued efficacy after discontinuation of therapy in the CBT group only. A study by Jacobs et al comparing zolpidem with CBT showed continued efficacy for the patients treated with CBT.
[68]

A European study by Sivertsen and colleagues showed that CBT was superior to zopiclone (not available in the United States). In fact, zopiclone was found to be no different from placebo on 3 of 4 outcome measures.
[74] CBT, on the other hand, reduced total awake time by 52%, improved sleep efficiency, and increased slow-wave sleep. At 6 months, sleep efficiency was still improved with CBT. The limitation of this study was that it consisted of 44 older individuals using zopiclone.

Efficacy of combined CBT and sedative-hypnotics

Several studies have demonstrated that after 10-24 months’ follow-up, patients in the CBT group demonstrated sustained benefit that was not seen in the combined CBT-hypnotic group. This could be because patients were less willing to practice CBT techniques during the initial phase if they obtained rapid, short-term improvement of sleep with a sedative-hypnotic. In this regard, many sleep experts feel that CBT should be considered as initial therapy for primary insomnia and adjunctive therapy for secondary insomnia.

CBT and hypnotic medications are efficacious for short-term treatment of insomnia, but few patients achieve complete remission with any single treatment. Morin et al studied 160 adults with persistent insomnia and demonstrated that CBT used singly or in combination with zolpidem produced significant improvements in sleep latency, time awake after sleep onset, and sleep efficiency during initial therapy.
[75]

Combined therapy produced a higher remission rate than CBT alone during the 6-month extended therapy phase and the 6-month follow-up period (56% vs 43%). Long-term outcome was optimized when medication was discontinued during maintenance CBT.
[75]

Previous

Next:

Pharmacologic Treatment of Insomnia

The pharmacologic treatment of insomnia has made great advances in the last 2 decades. In the early 19th century, alcohol and opioids were used as sleeping medications. In the late 19th century, chloral hydrate was used (and misused, in combination with alcohol, as “knockout drops” or a “Mickey Finn”). Barbiturates were used from the early 20th century until the early 1960s, when benzodiazepines (ie, flurazepam and quazepam) were first approved by the US Food and Drug Administration (FDA) for the treatment of insomnia.

In 2017, the American Academy of Sleep Medicine (AASM) released an updated guideline for the pharmacologic treatment of chronic insomnia in adults.
[6]

Benzodiazepines were commonly used until the 1980s, when tolerance, dependence, and daytime side effects were recognized as major limitations of these agents, particularly those with long elimination half-lives. Temazepam is still used for a short-term course (ie, from days to 1-2 weeks), at a dose of 15-30 mg at bedtime.

In the 1990s, antidepressants were widely used for primary insomnia, and they continue to be widely used, despite the fact that few randomized, controlled trials have demonstrated their efficacy in treating primary insomnia. At present, sedative-hypnotics remain the most commonly prescribed sleep medications.

Sedative-hypnotic drugs

Sedative-hypnotic medications do not usually cure insomnia, but they can provide symptomatic relief as sole therapy or as an adjunct with CBT. Furthermore, some patients cannot adhere to or do not respond to CBT and are candidates for these agents. The nonbenzodiazepine receptor agonists (eg, eszopiclone, zolpidem, zaleplon) are believed to be less habit-forming than benzodiazepines and, therefore, represent important advances in the long-term treatment of chronic insomnia.

The most appropriate use of nonbenzodiazepine receptor agonists is for transient and short-term insomnia in combination with nonpharmacologic treatment. Most authorities now agree that they should infrequently be the only therapy for chronic insomnia.

In the past, most studies of the efficacy of sedative-hypnotics had been short-term trials, generally less than 4 weeks. Use for longer than 4 weeks was thought to result in tolerance and decreased efficacy, although supportive findings are scarce, and the epidemiologic literature suggests that patients report continued efficacy with continued use. Nevertheless, because of the addictive nature of benzodiazepines, most authorities believe that the duration of use of these drugs should be limited.

Studies have indicated, however, that nonbenzodiazepine receptor agonists can have long-term efficacy for 6-12 months without the development of tolerance. Eszopiclone, the first sedative-hypnotic to be tested over a 6-month period, showed continued efficacy with nightly use over that period, with improved quality of life, reduced work limitations, and reduced global insomnia severity.
[76, 77] Another study demonstrated continued efficacy at 12 months.
[78]

Krystal et al showed long-term efficacy and safety of sustained-release zolpidem (Ambien-CR) for 6 months in a double-blind, placebo-controlled trial.
[79] Zolpidem can be used at a dose of 5 or 10 mg at bedtime for sleep-onset insomnia; zolpidem-controlled release can be used at doses of 6.25 or 12.5 mg for patients with sleep-maintenance insomnia or patients with both sleep-onset and sleep-maintenance insomnia.

Lower zolpidem doses were recommended by the FDA in January 2013, owing to the risk of next-morning mental impairment.
[80, 81] Data show that zolpidem blood levels may remain high enough the morning after nighttime usage to impair activities that require alertness, including driving. This next-morning impairment is highest for the controlled-release dosage form and is more prevalent in women because of their slower elimination compared with men.

The revised labeling for zolpidem recommends that the initial dose for immediate-release zolpidem products (Ambien and Edluar) be 5 mg for women and either 5 mg or 10 mg for men. The recommended initial dose for extended-release zolpidem (Ambien CR) is 6.25 mg for women and either 6.25 or 12.5 mg for men. The FDA also added a warning against driving or other activities requiring mental alertness the day after taking extended-release zolpidem at the 6.25-mg or 12.5-mg dose, because drug levels can remain high enough to impair these activities.
[82, 81]

Eszopiclone has a half-life of 5-7 hours and can be used for sleep-maintenance insomnia. The starting dose is 1 mg immediately before bedtime, with at least 7-8 hours remaining before the planned time of awakening. The dose may be increased if clinically warranted to 2-3 mg HS in nonelderly adults, and 2 mg in elderly or debilitated patients. Next-day impairment can occur after taking after a starting dose of 2 mg. FDA findings from observing 91 healthy adults showed that individuals who took a 3 mg dose of eszopiclone displayed severe psychomotor and memory impairment 7.5 hours later and that driving skills, memory, and coordination could remain impaired up to 11 hours later.
[11]

Zaleplon has a very short half-life (1 hr) and is indicated for sleep-onset insomnia at doses ranging from 5-20 mg. It can also be used for sleep-maintenance insomnia if taken at the time of awakening during the night. However, the patient should allow at least 4 hours for remaining sleep to avoid possible daytime sedation.

The following general precautions should be taken when using sedative-hypnotics:

Therapy should be instituted with a low dose and maintained at the lowest effective dose

Continued nightly use should be avoided; patients should be encouraged to use them only when truly necessary

Hypnotics with a rapid onset of action, such as zolpidem or zaleplon, are preferable when the problem is falling asleep

If the problem is staying asleep, a hypnotic with a slower rate of elimination may be more appropriate (eg, temazepam, estazolam, flurazepam)

If the patient is depressed, an antidepressant with sedative properties, such as trazodone, mirtazapine, or amitriptyline, may be preferable to a hypnotic

Hypnotics should never be used with alcohol

In general, pregnancy is a contraindication

Benzodiazepines should be avoided in patients with known or possible sleep apnea

Lower doses should be used in elderly patients

Long-term hypnotic pharmacotherapy may be necessary in patients with severe or treatment-resistant insomnia or chronic comorbid disorders, but follow-up must include regular assessment of necessity, efficacy, and adverse effects.
[1] Long-term administration of hypnotics may be intermittent, as needed, or nightly.
[1] If possible, during long-term therapy, patients should receive an adequate trial of CBT.
[1]

These agents should be used with caution in patients with a history of insufficient sleep syndrome, particularly in patients prone to alcohol use, since this group can be predisposed to the development of parasomnias (eg, sleep-walking or sleep-related eating disorder
[83, 84] )

In most patients, the risk of dependency is low. Few patients escalate the dose or use the drug more frequently than prescribed. Roehrs et al found no dose escalation after 12 months of nightly use of zolpidem by patients with primary insomnia.
[85] Nevertheless, sedative-hypnotics should be avoided in patients with a history of substance abuse.

Rebound insomnia may develop when a sedative-hypnotic is abruptly withdrawn. This is more likely to occur with larger doses and with the short-acting agents. Using smaller doses and tapering the drug can avoid rebound insomnia. The AASM guideline states that these measures are aided by concurrent CBT for insomnia (CBT-I).
[1, 6]

Suvorexant

Suvorexant (Belsomra) was approved by the FDA in August 2014 and is the first orexin receptor antagonist for insomnia. It is indicated for the treatment of insomnia characterized by difficulties with sleep onset and/or sleep maintenance. The orexin neuropeptide signaling system is a central promoter of wakefulness. Blocking the binding of wake-promoting neuropeptides orexin A and orexin B to receptors OX1R and OX2R by suvorexant is thought to suppress wake drive. Approval was based on three clinical trials involving more than 500 participants. The recommended dose is 10 mg for most patients. After taking 20 mg, impairment of next-day driving was observed.

The American Academy of Sleep Medicine (AASM) recommends that suvorexant be used as a treatment for sleep maintenance insomnia as opposed to no treatment.
[6]

Ramelteon

Ramelteon (Rozerem), a melatonin receptor agonist, is approved by the FDA for use in persons with insomnia. It has been shown to have no potential for abuse and, as such, is the first nonscheduled prescription drug available in the United States for the treatment of insomnia.

Ramelteon is a specific melatonin receptor agonist that binds to the melatonin MT1 and MT2 receptors. It has a half-life of 1-3 hours. The MT1 receptor attenuates the alerting signal of the suprachiasmatic nucleus (SCN) clock, and the MT2 receptor phase shifts (advances) the SCN clock to promote sleep.

Controlled trials have shown a decrease in sleep latency but no change in wake time after sleep onset and no next-morning residual effects. Additionally, studies thus far on elderly patients have shown no impairment in night balance, mobility, or memory.
[86, 87, 88]

This medication is suited for patients with sleep-onset insomnia, particularly for elderly patients with gait disorders who have an increased risk of falls and in patients with a history of substance abuse. The typical starting dose is 8 mg before bedtime. Ramelteon is not effective for sleep-maintenance insomnia. The AASM recommends ramelteon for the treatment of sleep onset insomnia (versus no treatment).
[6]

Sedating antidepressants

Although there is a paucity of clinical data on the use of sedating antidepressants for the treatment of primary insomnia without mood disorders, these agents are still sometimes used. Sedating tricyclic antidepressants, such as amitriptyline, nortriptyline, and doxepin, and the tetracyclic drug mirtazapine have been used.

Many clinicians believe that sedating antidepressants have fewer adverse effects than nonbenzodiazepine receptor agonists; however, this is not the case. Tricyclic drugs and mirtazapine can cause daytime sedation, weight gain, dry mouth, postural hypotension, and cardiac arrhythmias. Trazodone can cause priapism in men, daytime sedation, and hypotension.

The efficacy and safety of low-dose doxepin have been demonstrated in 2 randomized, double-blind, parallel-group, placebo-controlled trials. Low-dose doxepin is thought to be a hypnotic that primarily works through an antihistaminic effect.

Roth et al reported that low-dose doxepin (6 mg) provided significant improvements in sleep onset, maintenance, duration, and quality, as well as appearing to reduce early morning awakenings. These researchers used a first-night effect combined with a 3-hour phase advance to induce transient insomnia in healthy adults. The incidence of adverse events was comparable to placebo.
[89] .

In a 12-week study of elderly patients with chronic primary insomnia, Krystal et al reported that a nightly 1-mg or 3-mg dose of doxepin resulted in significant and sustained improvements in most insomnia endpoints, including sleep maintenance and early morning awakenings. There was no evidence of next-day residual sedation or other significant adverse effects. Efficacy was assessed using polysomnography, patient reports, and clinician ratings.
[90]

Antihistamines

Antihistamines are the major ingredient of over-the-counter (OTC) sleep aids and are the ingredient in cold and sinus formulas sold as bedtime-use medications. Nevertheless, common antihistamines (ie, first-generation H1-receptor antagonists such as diphenhydramine, hydroxyzine, and doxylamine) are not indicated for the treatment of sleeplessness.

While H1 antihistamines have sedative effects in healthy individuals, no study has established an effective dose range for these agents’ hypnotic effect in patients with insomnia. These agents may have some subjective benefit, but long-term efficacy and safety have not been demonstrated. Thus, their regular use in individuals with insomnia is not advised.
[6]

Melatonin

Melatonin has also become a popular OTC sleep aid. Melatonin is a naturally occurring hormone secreted by the pineal gland. The concentration of melatonin is highest in the blood during normal times of sleep and lowest during normal times of wakefulness. The general consensus is that melatonin given during normal waking hours has hypnotic properties.

However, the timing of evening administration is critical as to whether a hypnotic or chronobiologic effect occurs. Melatonin given early in the evening appears to increase sleep time; however, administration 30 minutes before a normal bedtime has not resulted in a decreased sleep latency or an increase in sleep time.

Most studies of melatonin have been small and of limited duration, and the results have conflicted somewhat, with several studies showing limited or no effect.
[18] Most of the data, however, seem to suggest that melatonin taken before bedtime decreases sleep latency, may increase total sleep time,
[92, 93] and may entrain irregular circadian rhythms.

Studies of melatonin in individuals with chronic insomnia have not demonstrated objective changes in patient sleep habits or changes in mood or alertness the day after treatment. In addition, a dose-response relationship has not been determined. OTC melatonin is also sold at doses much higher than those that naturally occur in the blood. The 2008 AASM guideline notes a relative lack of safety data and efficacy data and, therefore, states that melatonin is not recommended for the treatment of chronic insomnia.
[1]

Some studies, however, suggest a possible role for melatonin in the elderly. In a 2010 study, Wade et al determined that prolonged-release melatonin (2 mg) improved sleep latency and additional sleep and daytime parameters in patients 65 years of age and older. These improvements were maintained or enhanced over a 6-month period, with no signs of tolerance.
[94]

A double-blind, placebo-controlled clinical trial by Rondanelli et al in residents of a long-term care facility found that a nighttime dose of melatonin, combined with magnesium and zinc, appeared to improve residents’ quality of sleep and quality of life. The supplement, containing 5 mg melatonin, 225 mg magnesium, and 11.25 mg zinc, was administered 1 hour before bedtime.
[95]

Melatonin is not recommended by the AASM for sleep onset or sleep maintenance insomnia.
[6]

Alternative and herbal medications

Alternative and herbal medications have also been tried in the treatment of insomnia. Valerian root extract is the most widely used and studied of these agents. A 2006 meta-analysis of 16 randomized, controlled trials of valerian for the treatment of insomnia had conflicting results.
[96] The pooled data did seem to show evidence of improved sleep; however, the authors noted a possible publication bias that may have contributed to this result.

A 2010 met-analysis of 18 randomized, controlled trials of valerian for the treatment of insomnia detected no publication bias. However, although the results suggested that valerian may be effective for subjective improvement of insomnia, its effectiveness has not been demonstrated with quantitative or objective measurements.
[97]

A randomized, placebo-controlled trial by Taavoni et al found that valerian improves the quality of sleep in women with menopause who are experiencing insomnia. Patients in the treatment arm received 530 mg of concentrated valerian extract twice a day for 4 weeks.
[98]

Other herbal remedies such as chamomile and St. Johns wort have not shown efficacy for insomnia. Furthermore, potential risks have been associated with the use of some OTC remedies, such as dogwood, kava kava, alcohol, and L-tryptophan.
[99] For these reasons, the 2017 AASM guideline states that valerian and other alternative or herbal medications are not recommended for treatment of chronic insomnia.
[6]

Previous

Next:

Acupressure for Insomnia

A longitudinal study by Sun et al found that acupressure treatment can improve insomnia, with effects lasting after the end of intervention. In a randomized, controlled trial of 50 residents in long-term care facilities, 5 weeks of standard acupressure on the HT7 (Shenmen) points of both wrists significantly reduced insomnia, with the benefit persisting for up to 2 weeks afterward.
[100]

Previous

Next:

Devices

In June 2016, the FDA approved a prescription device for patients with insomnia, the Cerêve Sleep System, that helps reduce latency to stage 1 and stage 2 sleep by keeping the forehead cool. This device came about as a result of studies that showed that in patients with insomnia, the frontal cortex stays active, preventing them from getting deeper, more restorative sleep. The system consists of a bedside device controlled by software that cools and pumps fluid to a forehead pad that the patient wears throughout the night. Approval was based on three clinical studies that included more than 230 patients over 3800 research nights.
[101]

Previous

Next:

Diet and Exercise

Dietary measures in patients with insomnia are matters of timing and avoidance. The following recommendations may be useful:

Avoid caffeinated beverages in the late afternoon or evening, since the stimulant activity of adenosine antagonism can promote hyperarousal

Avoid alcohol in the evening, since this can worsen sleep-disordered breathing leading to frequent arousals; furthermore, while alcohol promotes sleep early in the night, it leads to more sleep disruption later in the evening

Exercise in the late afternoon or early evening (at least 6 hours before bedtime) can promote sleep. However, vigorous physical activity in the late evening (< 6 hours before bedtime) can worsen insomnia.

Previous

Next:

Treatment of Insomnia in Elderly Patients

The satisfaction of sleep declines with age. This probably is related to changes in sleep associated with age, such as a decrease in slow-wave sleep, increased time awake after sleep onset, and a tendency to go to bed early and rise early. Although napping is highly prevalent among elderly persons, it has not been consistently correlated with sleep disturbance.
[102]

However, aging should not be assumed to be the explanation for insomnia.
[103] Multiple factors affect sleep in the elderly, including nocturia, pain syndromes, and many medical disorders (eg, heart failure, chronic obstructive pulmonary disease, Parkinson disease). Other factors include restless legs syndrome, sleep apnea (all of which have increased frequency in the elderly), dementia, and, frequently, changing situational factors such as retirement, bereavement, or financial difficulties, which lead to anxiety and depression.
[104]

As in younger patients, nonpharmacologic treatment should take precedence over pharmacologic treatment. Psychological and behavioral interventions are effective in older adults, according to the 2008 AASM guideline.
[1] A 16-week randomized, controlled trial by Reid et al found that aerobic activity plus sleep hygiene improved sleep quality, mood, and quality of life in older adults with chronic insomnia.
[105]

In elderly patients, hypnotics should be prescribed cautiously and in lower doses than for younger patients. Drugs tend to have a longer duration of effect in elderly patients as a result of changes in metabolism and elimination. This can lead to an increased incidence of falls and resulting bone fractures at night (if the patient gets up to use the bathroom when not fully awake or ataxic) and decrements in daytime alertness and performance (including increased incidence of motor vehicle accidents).

Previous

Next:

Consultations

Primary care physicians should be able to diagnose and treat transient or short-term insomnia. Chronic insomnia is often more difficult to treat, and referral to a specialist may be indicated. Patients with comorbid medical conditions may benefit from referral to the appropriate specialist.

Patients should be referred to a sleep specialist in the following cases:

In cases of primary insomnia, particularly if it is psychophysiologic insomnia and of long duration

The patient requires daily or near-daily sedative-hypnotics for insomnia for 30 days or more

Many sleep centers have a staff psychologist who specializes in treating insomnia. The advantages include experience in cognitive-behavioral techniques and providing sleep education, greater available time for the often-frequent follow-up that is needed, and the ability to ascertain whether other psychological factors are present that may need further evaluation by a psychiatrist.

Patients with a history of depression should be treated with an antidepressant or referred to a psychiatrist, based on the physician's comfort level in treating depression, the severity of depression, and the response to therapy. In addition, patients with a history of substance abuse or another major psychiatric disorder should also be referred to a psychiatrist.

Theoretical model of the factors causing chronic insomnia. Chronic insomnia is believed to primarily occur in patients with predisposing or constitutional factors. These factors may cause the occasional night of poor sleep but not chronic insomnia. A precipitating factor, such as a major life event, causes the patient to have acute insomnia. If poor sleep habits or other perpetuating factors occur in the following weeks to months, chronic insomnia develops despite the removal of the precipitating factor. Adapted from Spielman AJ, Caruso LS, Glovinsky PB: A behavioral perspective on insomnia treatment. Psychiatr Clin North Am. 1987 Dec;10(4):541-53.

Disclosure: GXC Global, Inc. Intellectual property rights Medical Director - company is to develop a seizure detecting device. No conflict with any of the Medscape Reference articles that I wrote or edited.